AMER1

Last update 08 May 2025

Basic Info

Synonyms

AMER1, APC membrane recruitment protein 1, FAM123B

+ [5]

Introduction

Regulator of the canonical Wnt signaling pathway. Acts by specifically binding phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2), translocating to the cell membrane and interacting with key regulators of the canonical Wnt signaling pathway, such as components of the beta-catenin destruction complex. Acts both as a positive and negative regulator of the Wnt signaling pathway, depending on the context: acts as a positive regulator by promoting LRP6 phosphorylation. Also acts as a negative regulator by acting as a scaffold protein for the beta-catenin destruction complex and promoting stabilization of Axin at the cell membrane. Promotes CTNNB1 ubiquitination and degradation. Involved in kidney development.

100 Clinical Results associated with AMER1

100 Translational Medicine associated with AMER1

0 Patents (Medical) associated with AMER1

188

Literatures (Medical) associated with AMER1

01 May 2025·Computer Methods and Programs in Biomedicine

Intra-clustering analysis reveals tissue-specific mutational patterns

Article

Author: Choudalakis, Stamatis ; Kastis, George A ; Dikaios, Nikolaos

BACKGROUND AND OBJECTIVEThe identification of tissue-specific mutational patterns associated with cancer is challenging due to the low frequency of certain mutations and the high variability among tumors within the same cancer type. To address the inter-tumoral heterogeneity issue, our study aims to uncover infrequent mutational patterns by proposing a novel intra-clustering analysis.METHODSA Network Graph of 8303 patients and 198 genes was constructed using single-point-mutation data from The Cancer Genome Atlas (TCGA). Patient-gene groups were retrieved with the parallel use of two separate methodologies based on the: (a) Barber's modularity index, and (b) network dynamics. An intra-clustering analysis was employed to explore the patterns within smaller patient subgroups in two phases: i) to determine the significant presence of a gene with a cancer type using the Fisher's exact test and ii) to determine gene-to-gene patterns using multiple correspondence analysis and DISCOVER. The results are followed by a Benjamini-Hochberg false discovery rate of 5%.RESULTSThis analysis was applied over 24 statistically meaningful groups of 2619 patients spanning 21 cancer types and it recovered 42 mutational patterns that are not reported in the TCGA consortium publications. Notably, our findings: (i) suggest that AMER1 mutations are a putative separative element between colon and rectal adenocarcinomas, (ii) highlight the significant presence of RAC1 in head and neck squamous cell carcinoma (iii) suggest that EP300 mutations in head and neck squamous cell carcinoma are irrelevant of the HPV status of the patients and (iv) show that mutational-based clusters can contain patients with contrasting genetic alterations.CONCLUSIONSThe proposed intra-clustering analysis extracted statistically significant relationships within clusters, uncovering putative clinically relevant connections and disentangling mutational heterogeneity.

01 Mar 2025·iScience

WTX-L/β-arrestin2/LCN2 axis controls vulnerability to ferroptosis in gastric cancer

Article

Author: Zhang, Yiqiong ; Xu, Yangwei ; Huang, Weiye ; Wu, Hongmei ; Wang, Chuangyuan ; Zhang, Qingling ; Cai, Guixing ; Sun, Jingbo ; Qian, Xuexia ; Lin, Zhihao

Gastric cancer (GC) is one of the most prevalent and lethal cancers worldwide. Ferroptosis is a form of iron-dependent regulated cell death emerging as a promising strategy for cancer therapy, whereas the regulation mechanism remains unclear. WTX has been recognized as a potential tumor suppressor, but attempts at targeted therapy have not achieved substantial progress. Further research into the structure, function, and mechanisms is urgently needed. Herein, we identified a long isoform of WTX (WTX-L) as a potent ferroptosis effector in GC. Mechanistically, WTX-L competitively interacts with β-arrestin2, disrupting its direct binding to IκBα and subsequently activating the NF-κB/LCN2 pathway. LCN2 further triggers ferroptosis by significantly increasing the labile Fe²⁺ pool and promoting excessive lipid peroxidation. Blockade of the WTX-L/β-arrestin2/NF-κB/LCN2 axis significantly diminished the activity of ferroptosis inducers (erastin and RSL3) in vivo. Collectively, these findings reveal that targeting the ferroptosis vulnerabilities through WTX-L may represent a promising strategy for GC.

01 Dec 2024·Clinical Lung Cancer

Mutations Associated With High-Grade irAEs in NSCLC Patients Receiving Immunotherapies

Article

Author: Smith, Margaret R. ; Smith, Margaret R ; Su, Jing ; Ruiz, Jimmy ; Wang, Yuezhu ; Mileham, Kathryn F ; Mileham, Kathryn F. ; Miller, Lance D. ; Grayson, Jason M. ; Grayson, Jason M ; Xing, Fei ; D'Agostino, Ralph ; Chan, Michael D. ; Miller, Lance D ; Dixon, Caroline B. ; Dixon, Caroline B ; Oliver, George ; Liu, Yin ; Farris, Michael ; Lycan, Thomas ; Topaloglu, Umit ; Chan, Michael D ; Li, Wencheng

OBJECTIVESCompared to low-grade irAEs, high-grade irAEs are more often dose-limiting and can alter the long-term treatment options for a patient. Predicting the incidence of high-grade irAEs would help with treatment selection and therapeutic drug monitoring.MATERIALS AND METHODSWe performed a retrospective study of 430 stage III and IV patients with non-small cell lung cancer (NSCLC) who received an immune checkpoint inhibitor (ICI), either with or without chemotherapy, at a single comprehensive cancer center from 2015 to 2022. The study team retrieved sequencing data and complete clinical information, including detailed irAEs medical records. Fisher's exact test was used to determine the association between mutations and the presence or absence of high-grade irAEs. Patients were analyzed separately based on tumor subtypes and sequencing platforms.RESULTSHigh-grade and low-grade irAEs occurred in 15.2% and 46.2% of patients, respectively. Respiratory and gastrointestinal irAEs were the 2 most common irAEs. The distribution of patients with or without irAEs was similar between ICI and ICI+chemotherapy-treated patients. By analyzing the mutation data, we identified 5 genes (MYC, TEK, FANCA, FAM123B, and MET) with mutations that were correlated with an increased risk of high-grade irAEs. For the adenocarcinoma subtype, mutations in TEK, MYC, FGF19, RET, and MET were associated with high-grade irAEs; while for the squamous subtype, ERBB2 mutations were associated with high-grade irAEs.CONCLUSIONThis study is the first to demonstrate that specific tumor mutations correlate with the incidence of high-grade irAEs in patients with NSCLC treated with an ICI, providing molecular guidance for treatment selection and drug monitoring.

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AMER1

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